Publications by authors named "P Coburn"
Purpose: The purpose of this study was to explore the therapeutic potential of the novel combination of Bacillus bacteriophage lysin (PlyB) and a synthetic TLR2/4 inhibitor (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine, OxPAPC) in the treatment of experimental Bacillus cereus endophthalmitis.
Methods: C57BL/6J mice were injected with 100 colony forming units (CFUs) Bacillus cereus to induce endophthalmitis. Two hours postinfection, groups of mice were treated with either PlyB, PlyB with OxPAPC, or the groups were left untreated to serve as a control.
Article Synopsis
- Extracellular vesicles (EVs) play a key role in how muscles and fat communicate, particularly after resistance exercise.
- A study found that muscle-specific microRNA-1 (miR-1) is transferred to fat tissue through EVs after weightlifting sessions.
- The research highlights how miR-1 affects fat cell behavior by regulating target genes related to fat breakdown, suggesting a mechanism for how exercise influences fat metabolism.
Purpose: To test the hypothesis that (C-C motif) ligand 2 (CCL2) and CCL3 impact retinal function decline and inflammation during Staphylococcus aureus endophthalmitis.
Methods: Experimental endophthalmitis was initiated by intravitreal injection of 5000 colony-forming units of S. aureus into the eyes of C57BL/6J, CCL2-/-, or CCL3-/- mice.
Background: can cause self-limiting gastrointestinal infections, but when infecting the eye, can cause rapid and irreversible blindness. This study investigated whether clinical ocular and gastrointestinal isolates differed in terms of virulence-related genotypes and endophthalmitis virulence.
Methods: Twenty-eight ocular, gastrointestinal, and laboratory reference isolates were evaluated.
Patients with Lafora disease have a mutation in EPM2A or EPM2B, resulting in dysregulation of glycogen metabolism throughout the body and aberrant glycogen molecules that aggregate into Lafora bodies. Lafora bodies are particularly damaging in the brain, where the aggregation drives seizures with increasing severity and frequency, coupled with neurodegeneration. Previous work employed mouse genetic models to reduce glycogen synthesis by approximately 50%, and this strategy significantly reduced Lafora body formation and disease phenotypes.
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